Much of the pathophysiology of Parkinson's disease, and other movement disorders, has been localized to the basal ganglia, especially to the striatum. However, very little is known about the normal and abnormal function of the striatum, except that it is a significant motor structure. The working hypotheses are that the striatum processes information from several sensory modalities including somatosensory information, that dopamine plays a major role in the striatal processing of a repetitive somatosensory stimulus by decreasing "surround" activity, as it does in the fish retina to help define a receptive field, that this action of dopamine may be a mechanism for selection of stimuli and somatotopic localization in the motor system. Thus in Parkinson's disease the striatum may not be able to give the cortex the precise information it needs to plan and carry out a movement. The methods used are 14C deoxyglucose autoradiography, neurotoxic lesions, peripheral drug injections, tactile stimulation, induced and trained movements. We have already found that forelimb tactile stimuli affect striatal glucose utilization. Tactile stimuli will be applied to the hindlimb to demonstrate the specificity of anatomic localization in striatum. Tactile stimuli will be applied in animals with a cortical lesion to learn whether the origin of the somatosensory response in striatum is in cortex. Tactile stimuli will also be applied in animals with striatal dopamine- depleting lesions, in animals treated with L-dopa, and in animals treated with a dopamine antagonist to confirm the role of dopamine in striatum as a "sharpener" of tactile information. Finally, the effect of movement will be mapped in striatum to learn whether regions of increased glucose utilization are separate from and/or overlap with somatosensory regions, and whether a decreased surround pattern exists as for somatosensory information.